IFITM3通过P38-MAPK/EMT信号轴对胃癌细胞的影响

Effect of IFITM3 on Gastric Cancer Cells through p38-MAPK/EMT Signaling Axis

目的 探究IFITM3在胃癌中的表达及其对胃癌细胞恶性生物学行为的影响。方法 利用数据库分析IFITM3在胃癌中的表达及分析IFITM3与胃癌患者总体生存率的相关性;在胃癌细胞SGC-7901中转染siIFITM3,利用CCK-8实验、流式细胞术和伤口愈合实验分别分析细胞增殖、凋亡及迁移。Western blot检测P38-MAPK磷酸化水平和EMT相关蛋白(E-cadherin、Snail和Vimentin)的表达。结果 IFITM3在胃癌中高表达且与胃癌患者总体生存率负相关;在SGC-7901细胞中转染si-IFITM3能有效敲低IFITM3的表达;敲低IFITM3能显著抑制细胞增殖和迁移,诱导细胞凋亡,同时也能减少P38-MAPK的磷酸化和EMT相关蛋白的表达。结论 敲低IFITM3能通过减少P38-MAPK蛋白磷酸化,抑制胃癌细胞EMT,从而减缓细胞增殖和迁移,诱导细胞凋亡。

Objective To investigate the egression of IFITM3 in gastric cancer and its effect on malignant biological behavior of gastric cancer cells.Methods The egression of IFTTM3 in gastric cancer was analyzed by database and the correlation between IFITM3 and overall survival rate of gastric cancer patients was analyzed Si-ifitm3 was transfected into GASTRIC cancer cells SGC-7901,and cell proliferation,apoptosis and migration were analyzed by CCK-8 assay,flow cytometry and wound healing assay The phosphoiylation ofP38-MAPK and the egression of EMT-related proteins(e-cadherin,Snail and Wnentin)were detected by Western blot Results 1PH M3 was highly expressed in gastric cancer and negatively correlated with the overall survival rate of gastric cancer patients.Transfection of SMFITM3 in SGC-7901 cells could effectively knock down the expression of 1P1TM3.Knocking down IFITM3 can significantly inhibit cell proliferation and migration,induce cellptosis,and also reduce the phosphorylation of P38-MAPK and the expression of EMT-related proteins.Conclusion Knockdown lhl l M3 can inhibit EMT of gastric cancer cells by reducing phosphorylation of P38-MAPK protein,thus slowing down cell proliferation and migration,and inducing cell apoptosis.